Evidence map›Paper›PMID 32064156›Full record

ArticleAmerican journal of cancer research2020

TRIM21 overexpression promotes tumor progression by regulating cell proliferation, cell migration and cell senescence in human glioma.

Zhipeng Zhao, Yuqi Wang, Dapeng Yun, Qilin Huang, Delong Meng, Qing Li, Pingzhao Zhang, Chenji Wang, Hongyan Chen, Daru Lu

Open access · greenAbstract read
In one paragraph

Article in American journal of cancer research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
3.5field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

45 citing papers in PubMed, 61 citations in OpenAlex.

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  8. Breast Cancer Incidence in Sjögren Syndrome Patients.Journal of clinical medicine · 2025
    Article
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  10. Targeting the TRIM21-PD-1 axis potentiates immune checkpoint blockade and CAR-T cell therapy.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 6 institutions in 2 countries.

Zhipeng ZhaoState Key Laboratory of Genetic Engineering and MOE Engineering Research Center of Gene Technology, School of Life Sciences, Fudan University Shanghai 200438, China.
Yuqi WangState Key Laboratory of Genetic Engineering and MOE Engineering Research Center of Gene Technology, School of Life Sciences, Fudan University Shanghai 200438, China.
Dapeng YunDepartment of Pharmacology, The University of Texas Southwestern Medical Center Dallas TX75390, USA.
Qilin HuangDepartment of Neurosurgery, Shanghai Institute of Neurosurgery, Changzheng Hospital, Second Military Medical University Shanghai 200003, China.
Delong MengDepartment of Molecular Biology, The University of Texas Southwestern Medical Center Dallas TX75390, USA.
Qing LiShanghai Center for Clinical Laboratory 528 Hongshan Road, Pudong District, Shanghai 200126, China.
Pingzhao ZhangFudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Shanghai Medical College Shanghai 200032, China.
Chenji WangState Key Laboratory of Genetic Engineering, Collaborative Innovation Center for Genetics and Development, School of Life Sciences, Fudan University Shanghai 200438, China.
Hongyan ChenState Key Laboratory of Genetic Engineering and MOE Engineering Research Center of Gene Technology, School of Life Sciences, Fudan University Shanghai 200438, China.
Daru LuState Key Laboratory of Genetic Engineering and MOE Engineering Research Center of Gene Technology, School of Life Sciences, Fudan University Shanghai 200438, China.
Fudan University · CNThe University of Texas Southwestern Medical Center · USFudan University Shanghai Cancer Center · CNSecond Military Medical University · CNShanghai Clinical Research Center · CNXizang Minzu University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Molecular biomarkers combined with histopathological examination are of critical importance in the diagnosis and treatment of gliomas. Although recent studies have shown that many tripartite motif-containing (TRIM) family proteins could regulate the cell cycle, cell proliferation, and differentiation in cancers, the precise role of TRIM21 has been unknown in glioma. In this study, we analyzed TRIM21, which was upregulated in gliomas and identified its role in tumor proliferation, migration and drug resistance. By using immunohistochemical analysis, we found that the expression level of TRIM21 was upregulated in glioma specimens and the higher expression level of TRIM21 was associated with poorer clinical outcomes in glioma patients. Moreover, we demonstrated that TRIM21 could act as a regulator of the proliferation, cell cycle, and migration of glioma cells by gain- and loss-of function assays in vitro. In vivo, TRIM21 could also modulate glioma progression in murine intracranial xenografts. Furthermore, we found that TRIM21 suppressed cellular senescence via the p53-p21 pathway, and increased drug resistance in glioma cells by RNA-seq analysis, SA-

Indexed as

cell senescencedrug resistanceGliomap53-p21 pathwayprognosisTRIM21

Identifiers

PMID32064156
PMCPMC7017742
OpenAlexW3007042881

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.